Circulating Growth Hormone (GH), Insulin-like Growth Factor-I (IGF-I) and Free Thyroxine, GH Response to Clonidine Provocation and CT Scanning of the Hypothalamic-pituitary Area in Children with Sickle Cell Disease
Autor: | Nagwa El Banna, Maurice Asfour, Ashraf T Soliman, Assim Darwish, H Mohammed, Mohammed R Bassiony |
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Rok vydání: | 1995 |
Předmět: |
Male
medicine.medical_specialty Pituitary gland Oman medicine.medical_treatment Hypothalamus Growth Short stature Clonidine Insulin-like growth factor Internal medicine medicine Humans Insulin-Like Growth Factor I Child Hydrocortisone business.industry Thyroxine Somatropin Infectious Diseases medicine.anatomical_structure Endocrinology Case-Control Studies Growth Hormone Pituitary Gland Pediatrics Perinatology and Child Health Female Hemoglobin SC Disease Hypothalamic pituitary axis medicine.symptom Tomography X-Ray Computed business Hormone medicine.drug |
Zdroj: | Journal of Tropical Pediatrics. 41:285-289 |
ISSN: | 1465-3664 0142-6338 |
DOI: | 10.1093/tropej/41.5.285 |
Popis: | Serum growth hormone (GH), cortisol, free thyroxine (FT4), thyroid-stimulating hormone (TSH), and insulin like growth factor I (IGF-I) concentrations were measured in 15 children with sickle cell disease (SCD) together with their heights5th percentile for age and gender, and in 15 healthy age-matched children who had normal variant short stature (NVSS). GH response to an oral dose of clonidine (0.15 mg/m2) and cortisol response to ACTH stimulation were determined in the two groups. Children with SCD had significantly lower serum concentrations of IGF-I and decreased GH response to stimulation. Eight out of the 15 children with SCD did not mount an appropriate GH response to clonidine provocation (10 micrograms/l). CT scanning of the hypothalamic-pituitary area in those eight children with SCD revealed a partial or complete empty sella in all of them. It appears that defective GH release, and consequently low IGF-I production and slow growth velocity in children with SCD might be secondary to hypoxic-vascular insults to their hypothalamic-pituitary axis during one or more of the sickling episodes. |
Databáze: | OpenAIRE |
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